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This hypothesis has been a major focus of research in the fields pathophysiology and pharmacotherapy for over 25 years [1] and led to the development of new classes of drugs such as SSRIs (selective-serotonin reuptake inhibitors)[2]. This conceptual framework has been challenged within the scientific community, though no other demonstrably superior hypothesis has emerged. While the hypothesis has been shown to be simplistic and lacking, there is sufficient evidence to consider it as a useful heuristic in the aiding of our understanding of brain chemistry and explaining pharmacotherapy.[3][4] Wayne Goodman, Chair of the FDA Psychopharmacological Advisory Committee, has described the serotonergic theory of depression as a "useful metaphor" for understanding depression, though not one that he uses with his own psychiatric patients.[5] Recently, psychiatrist Peter Kramer stated that the serotonin theory of depression had been declared dead prematurely.[6] Kramer argues that recent scientific research actually shows a definitive role for serotonin deficiency in depression. An analysis of the studies Kramer cites argues that such statements are premature.[7]

In the 1950s the monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants were accidentally discovered to be effective in the treatment of depression[8]. These findings and other supporting evidence led Joseph Schildkraut to publish his paper called "The Catecholamine Hypothesis of Affective Disorders" in 1965.[9] Schildkraut associated low levels of neurotransmitters with depression. Research into other mental impairments such as schizophrenia also found that too little activity of certain neurotransmitters were connected to these disorders.